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ACEM Primary VIVA > VIVA: Physiology - Renal > Flashcards

VIVA: Physiology - Renal Flashcards

1
Q

What are the physiological consequences of impaired renal function?

A

3/4 to pass:
1. Proteinuria:
- Predominantly albuminuria
- Due to increased permeability of glomerular capillaries
2. Uraemia:
- Accumulation of breakdown products of protein metabolism resulting in symptoms of uraemia
3. Acidosis:
- Failure to excrete acid products of digestion/metabolism with urine maximally acidified
- Total amount of H+ secreted reduced due to impaired renal tubular production of NH4+
- Exception: renal tubular acidosis (impaired ability to acidify urine)
- Hyperkalaemia due to H+/K+ exchange
4. Abnormal Na+ handling (retains excess amounts Na+), due to three mechanisms:
- Acute glomerulonephritis: amount of Na+ filtered markedly decreased
- Nephrotic syndrome: increased aldosterone causes salt retention, low plasma proteins means fluctuating shifts from plasma into interstitium, resulting low plasma volume triggers RAAS
- Volume overload

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2
Q

What is the normal glomerular filtration rate?

A
  • 125ml/min* (180L/24hrs) in normal adult
  • 10% lower in females

*needed to pass

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3
Q

List some factors that affect the GFR

A
  1. Size of capillary bed:
    - Regulated by mesangial cells * (contractile cells) located in the glomerulus (between the basal lamina and the endothelium)
  2. Permeability of glomerular capillaries:
    - 50x that of skeletal muscle capillaries
  3. Hydrostatic and osmotic pressure gradients (Starling forces):
    - Oncotic pressure (plasma protein concentration)
    - Glomerular capillary hydrostatic pressure
  4. Systemic blood pressure
  5. Afferent arterial pressure (renal artery blood flow):
    - Kept stable by autoregulation between 90-210mmHg
  6. Afferent or efferent arteriolar constriction
  7. Hydrostatic pressure in Bowman’s capsule
  8. Intrarenal interstitial pressure:
    - Increased in ureteral obstruction, renal oedema
  9. Age

*needed to pass + 3 others

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4
Q

What substances act on mesangial cells to change GFR?

A
  1. Increase GFR*:
    - ANP
    - Dopamine
    - PGE2
    - cAMP
  2. Decrease GFR*:
    - Noradrenaline
    - Vasopressin
    - AT II
    - Histamine
    - PGF2
    - Endothelins
    - TxA2
    - Leukotrienes

*at least 1 of each and effect

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5
Q

Describe the neurological pathways involved in normal micturition

A
  • Sacral spinal reflex * mediated by S2, S3 and S4 nerve roots
  • Facilitated and inhibited by higher centres, and subject to voluntary control *
  • First urge to void occurs at 150ml
  • Marked fullness at 400ml with sudden rise in intravesical pressure triggering reflex contraction
  • Micturition reflex occurs via stretch receptors in bladder wall, with afferent limb in pelvic nerves
  • Parasympathetic efferent fibres * (via same pelvic nerves) mediate contraction of detrusor muscle
  • Pudendal nerve (S2, S3 and S4) permits voluntary contraction of perineal muscles and external urethral sphincter, to slow or halt flow
  • Sympathetic nerves to bladder play no role in micturition

*needed to pass

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6
Q

Describe the muscles involved in micturition

A
  1. Bladder:
    - Smooth muscle arranged in spiral, longitudinal and circular bundles
    - Circular bundle is called the detrusor muscle *
    - Contraction of detrusor is responsible for involuntary emptying
  2. External urethral sphincter *:
    - Skeletal muscle sphincter of the membranous urethra
    - Relaxes during micturition
    - This is voluntarily controlled
  3. Perineal muscles:
    - Relaxes during micturition
    - Also voluntarily controlled
  4. Bulbocavernosus muscle in males:
    - Several contractions of bulbocavernosus expels urine left in urethra
  5. Abdominal wall muscles:
    - Contraction aids expulsion of urine

NB: internal urethral sphincter (smooth muscle bundles passing on either side of urethra) plays no apparent role in micturition

*needed to pass

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7
Q

Describe the factors influencing angiotensin II production

A

AT II is the effector protein in the renin-angiotensin *, integral to the control of volume regulation *
Increased renin secretion due to:
- Increased sympathetic activity
- Increased circulating catecholamines
- Prostaglandins
- Above as a result of Na+ depletion, diuretics, hypotension, haemorrhage, dehydration, cardiac failure, cirrhosis, upright posture, renal artery and aortic constriction
Decreased renin secretion due to:
- Increased Na+ and Cl- reabsorption across macula densa
- Increased afferent arteriolar pressure
- Vasopressin

*needed to pass + 2 others

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8
Q

What are the physiological effects of angiotensin II?

A
  • Arteriolar constriction *
  • Acts directly on adrenal cortex to increase aldosterone
  • Facilitates release of NA
  • Contraction of mesangial cells causing decreased GFR
  • Direct effect on renal tubules to increase Na+ reabsorption
  • Acts on brain to decrease sensitivity of baroreceptor reflex, and to increase water intake and vasopressin and ACTH secretion (via the circumventricular organs)

*needed to pass + 2 others

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9
Q

How does the countercurrent mechanism enable the kidney to concentrate urine?

A
  • Concentrating mechanism depends on maintaining a gradient of increasing osmolality along medullary pyramids *
  • Gradient is produced by countercurrent multipliers in the loop of Henle, and maintained by the vasa recta acting as countercurrent exchangers *:
    1. Water moves out of the thin descending limb * via aquaporin 1
    2. Active transport of Na+ and Cl- out of thick ascending limb of loop of Henle *
    3. With continued inflow of isotonic fluid into the proximal tubule and out of the descending limb, water moves out of the collecting duct (into the hypertonic interstitium of the medullary pyramids) under the influence of ADH
  • Vasa recta acts as countercurrent exchangers in the kidney, in which NaCl and urea diffuse out of the scending limb of the vessel and into the descending limb, while water diffuses out of the descending into the ascending limb: as a result, the solute remains in the medullary pyramid to maintain the interstitial concentration

*needed to pass

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10
Q

What are the essential features of the loop of Henle countercurrent multiplier?

A

High permeability of the thin descending limb to water (via aquaporin 1), and active transport of Na+ and Cl- out of the thick ascending limb which is not permeable to water

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11
Q

What is the role of urea in the countercurrent mechanism?

A

Contributes to the osmotic gradient * in the medullary pyramids

*needed to pass

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12
Q

How does urea reach the interstitium?

A
  • Transported by urea transporters via facilitated diffusion *
  • Amount of urea depends on the amount filtered, which is influenced by dietary protein

*needed to pass

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13
Q

What is the definition of the glomerular filtration rate?

A

Amount of fluid (plasma filtrate) filtered by the glomerulus per unit time

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14
Q

What are mesangial cells?

A
  • Contractile cells * that help to regulate GFR *
  • Located between the basal lamina and the endothelium in the glomerulus *
  • Common between neighbouring capillaries, and in these locations the basal membrane forms a sheath shared by both capillaries
  • Also secrete the extracellular matrix, take up immune complexes, and are involved in the progression of glomerular disease

*needed to pass

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15
Q

What clinical factors alter Starling forces controlling glomerular filtration?

A

2 to pass:
- Alterations in renal blood flow
- Systemic BP
- Ureteric obstruction
- Renal parenchymal oedema
- Changes in plasma protein concentration
- Changes in the glomerular filtration coefficient (K), under control of mesangial cell contraction

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16
Q

How do the kidneys handle potassium?

A
  • Freely filtered at the glomerulus (600mmol/day) *
  • Majority (>90%) is reabsorbed in proximal tubules and thick ascending limb of the loop of Henle (560mmol/day) *: mainly due to passive resorption proportional to flow in proximal tubule, and active transport via Na-K-2Cl co-transporter in TAL of LoH
  • Secretion occurs in distal tubules * and collecting ducts as is approximately equal to K+ intake
  • The amount secreted is proportionate to flow rate through distal tubules (rapid flow rate prevents tubular K+ concentration rising and impairing passive secretion)
  • Excretion in collecting ducts is under influence of aldosterone (~90mmol/day), which increases K+ excretion via Na+/K+ ATPase
  • Small amount of K+ exchanged for H+ in collecting duct
  • Total secreted load averages 50mmol/day but varies with renal tubular flow and aldosterone level

*needed to pass

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17
Q

As well as filtration, by what other means does the kidney regulate the composition of urine?

A

Secretion and resorption

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18
Q

Describe a method for measuring the glomerular filtration rate

A
  • Measure excretion of a substance which is freely filtered * through the glomeruli *, but neither secreted * nor reabsorbed * by the tubules *
  • Non-toxic, not metabolised
  • E.g. inulin
  • GFR = (Ux x V / Px) where Ux = urinary concentration, V = urine flow per unit time, Px = arterial plasma concentration (if X not metabolised then venous can be substituted)

*3/5 to pass + example + basic formula

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19
Q

Describe how the kidney handles glucose

A
  • Freely filtered at the glomerulus *
  • Resorbed in the early part of the proximal convoluted tubule * by secondary active transport
  • Na+-dependent co-transportation * (SGLT2 into cells then GLUT2 facilitated diffusion into interstitial fluid)
  • Excreted in the urine if renal threshold * is exceeded

*needed to pass

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20
Q

What are the potential consequences of glycosuria?

A

Osmotic diuresis leading to dehydration and electrolyte loss (Na+, K+)

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21
Q

Where does the acidification of the urine occur? How is H+ secreted in each of those areas?

A
  1. Proximal tubule *:
    - Na-H exchange transporter * (one Na+ and one HCO3- reabsorbed for each H+ excreted)
  2. Distal tubule:
    - Secretion of H+ is independent of Na+
    - Via ATP-driven proton pump, stimulated by aldosterone
    - Also via H-K ATPase pump, and anion exchanger 1
  3. Collecting duct:
    - As for distal tubule

*needed to pass + 1 other site with mechanism

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22
Q

What is the limiting pH of urine and where is it reached?

A
  • The limiting pH is 4.5 * (1000x concentration in plasma)
  • It is the maximal H+ gradient that can be achieved in the tubules
  • It occurs in the collecting duct *
  • Possible due to presence of buffers (bicarbonate, dibasic phosphate, ammonia)

*needed to pass

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23
Q

How do the kidneys respond to a metabolic acidosis?

A
  • Aims to return serum pH to normal by increasing H+ excretion *
  • Kidney retains HCO3- by actively secreting H+ *
  • Renal tubule cells contain carbonic anhydrase converting CO2 to H+ and HCO3-, then PCT cells secrete H+ in exchange for Na+ *
  • In the DCT, H+ is secreted by a proton pump, limited by urinary pH >4.5 (limiting pH)
  • Buffering in tubular fluid pH with H2CO3, HPO4 and NH3 allows greater H+ secretion *
  • HCO3- is actively reabsorbed into the peritubular capillary

*needed to pass

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24
Q

What substances as urinary buffers for the excretion of H+?

A

2/3 to pass:
- NH3 forms NH4+
- HCO3 forms CO2 and H2O
- HPO4(2-) forms H2PO4

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25
Q

Besides renal excretion of H+, how else can the body compensate for metabolic acidosis?

A

Respiratory system * responds by increasing ventilation * which results in a decrease in pCO2, which causes increase in pH (this is a more rapid response than renal compensation)

*needed to pass

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26
Q

What happens to glutamine synthesis in the liver in chronic metabolic acidosis?

A

Glutamine synthesis increases * in liver, to provide kidney with additional source of NH3+ as well as NH3 secretion increasing over days

*needed to pass

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27
Q

What are the principal buffering systems in the body?

A

2/4 to pass:
- Blood: bicarbonate, protein, haemoglobin
- Interstitium: bicarbonate
- Intracellular: protein, phosphate
- Urine: bicarbonate, phosphate, ammonia

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28
Q

Outline how the body responds to a metabolic acid load

A
  1. Buffering in blood, interstitial and intracellular space *
  2. Respiratory response:
    - H2CO3 converted to H2O and CO2, CO2 expired via lungs * through increased minute ventilation
  3. Renal:
    - Renal mechanisms operate to compensate for metabolic acidosis and return serum pH towards normal
    - Anions that replace HCO3- are filtered at the glomerulus along with corresponding cations (mainly Na+)
    - Renal tubule cells secrete H+ into tubular fluid in exchange for Na+ and HCO3- *
    - Buffering in the urine gives greater capacity to this system (otherwise limiting pH of 4.5 would stop further H+ secretion) *
    - Buffering systems include bicarbonate, phosphate and ammonia *

*needed to pass

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29
Q

What factors increase acid secretion?

A

2/4 to pass:
- Increased pCO2
- Increased aldosterone
- Decreased K+
- Increased carbonic anhydrase concentration

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30
Q

How does aldosterone affect potassium excretion?

A
  • Aldosterone secretion is triggered by high serum K+
  • Aldosterone acts at collecting tubules to increase Na+ reabsorption and secrete K+ and H+ *
  • Effect is on principal cells in the collecting tubules
  • Na-K ATPase pump * in basolateral surface of principal cells results in 3x Na+ absorbed into bloodstream in exchange for 2x K+ into the principal cells
  • Higher intracellular K+ concentration drives K+ into tubular lumen via K+ channels in apical cell membrane
  • Na+ enters from tubular lumen via Na+ channels in apical membrane, and is pumped into the bloodstream via Na-K ATPase pump

*needed to pass

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31
Q

How does a metabolic acidosis affect potassium secretion?

A

In a metabolic acidosis state, H+ excretion is increased and K+ is reabsorbed in exchange, due to the action of H+ on H+-K+ ATPase in collecting duct cells

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32
Q

Explain K+ transport in the collecting duct

A
  • H+-K+ ATPase in the cells of the collecting ducts reabsorbs K+ in exchange for H+
  • Hence if H+ secretion is increased, K+ excretion is decreased
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33
Q

What other major ions are involved in K+ transport in the nephron?

A

Na+
H+

34
Q

What factors influence the kidney’s handling of K+?

A
  1. Rate of flow of tubular fluid through distal nephron *:
    - With rapid flow, the concentration of K+ in the fluid remains lower and secretion continues
  2. Increased delivery of Na+ to the collecting ducts promotes increased secretion of K+ (e.g. thiazide diuretics)
  3. Conversely decreased delivery of Na+ to the collecting ducts promotes decreased secretion of K+
  4. Inhibition of K+ absorption in the proximal nephron (e.g. osmotic or loop diuretics) promotes excretion of K+
  5. In the distal nephron K+ and H+ compete for secretion in association with reabsorption of Na+ *:
    - Therefore in acidosis with H+ excretion is increased, K+ secretion is decreased
  6. Aldosterone increases reabsorption of Na+ in the collecting ducts and thereby promotes K+ secretion *

*2/3 to pass

35
Q

How do the ascending and descending limbs of the loop of Henle differ in function?

A
  • Thin descending limb is water-permeable * (via aquaporins) and tubular fluid becomes hypertonic *
  • Thick ascending limb is impermeable to water, and Na+, K+ and Cl- are actively transported out so fluid ends up more hypotonic *
  • K+ diffuses back passively

*needed to pass

36
Q

Describe the process of tubuloglomerular feedback

A
  • This process aims to maintain the constancy of the load delivered to the distal tubule
  • The macula densa in the ascending limb of the loop of Henle senses the rate of flow and feeds back to either increase or decrease the rate of filtration in the glomerulus
37
Q

Outline the structure of the loop of Henle

A
  • Thin/descending and thick/ascending limbs
  • Situated mostly in the renal medulla
  • Origin from PCT *
  • Short (cortical; 85%) and long (juxtamedullary; 15%) loops
  • Macula densa at distal end, where it joins the DCT *

*needed to pass

38
Q

Describe the changes in the tonicity of tubular fluid as it moves along the loop of Henle

A
  • Fluid in the descending limb of the loop of Henle becomes hypertonic as water moves out of the tubule into the hypertonic interstitium
  • In the ascending limb it becomes more dilute because of the movement of Na+ and Cl- out of the tubular lumen
  • When fluid reaches the top of the ascending limb (the diluting segment), it is now hypotonic to plasma
39
Q

What prevents vesico-ureteric reflux?

A

Oblique passage of ureters through bladder wall * keeps ureters closed except during peristaltic waves

*needed to pass

40
Q

Describe the reflex control associated with voiding

A
  • The bladder smooth muscle has some inherent contractile activity: however, when its nerve supply is intact, stretch receptors in the bladder wall initiate a reflex contraction that has a lower threshold than the inherent contractile response of the muscle
  • Fibres in the pelvic nerves are the afferent limbs of the voiding reflex, and the parasympathetic fibres * to the bladder that constitute the efferent limb also travel in these nerves
  • The reflex is integrated in the sacral portion * of the spinal cord
  • In the adult, the volume of urine in the bladder than normally initiates a reflex contraction is about 300-400ml *
  • The sympathetic nerves to the bladder play no part in micturition: they do mediate the contraction of the bladder muscle that prevents semen from entering the bladder during ejaculation

*needed to pass

41
Q

Draw a nephron and describe the functions of each part

A
  1. Glomerulus:
    - Filtration
  2. Afferent arteriole:
    - Contain juxtaglomerular cells which secrete renin
  3. Capillary tuft:
    - Encapsulated in Bowman’s capsule
  4. Efferent arteriole
  5. Proximal convoluted tubule:
    - Resorption of most solute (Na+, glucose, amino acids, HCO3-)
  6. Descending limb of loop of Henle:
    - Thin and water permeable
  7. Thick ascending loop of Henle:
    - Site of Na+/K+/2Cl- transporter, responsible for generating concentration gradient
  8. Distal convoluted tubule:
    - Site of Na/Cl transporter
    - Proximal part is macula dense which forms the juxtaglomerular apparatus
  9. Collecting duct:
    - Principal cells: Na+ and H2O absorption under control of ADH and aldosterone
    - Intercalated cells: involved in H+ excretion
42
Q

Describe the cell types in the glomerus and their functions

A
  1. Capillary endothelial cells *:
    - Afferent arteriole becomes a tuft of capillaries invaginated into Bowman’s capsule
    - Endothelium is fenestrated with 70-90nm pores
    - Separated from capsule epithelium by basal lamina
  2. Epithelial cells of Bowman’s capsule *:
    - Podocytes possess pseudopodia * that interdigitate to form 25nm wide filtration slits * over capillary endothelium, with each slit enclosed by a thin membrane
    - Mesangial cells * are stellate and lie between capillary endothelium and basal lamina: they are involved in regulation of filtration, secretion of various substances, and absorption of immune complexes

*needed to pass

43
Q

What properties of substances in the blood prevent free passage across the glomerular membrane?

A
  • Large diameter >8nm
  • Lack of neutrality (charged)
44
Q

Explain how hypotension activates the renin-angiotensin system

A

Hypotension leads to reduced perfusion pressure of the afferent glomerular arteriole, stimulating release of renin by the juxtaglomerular cells

45
Q

How does the renin-angiotensin system contribute to the restoration of the blood volume?

A

4/5 to pass:
- Renin converts angiotensinogen to angiotensin I
- Angiotensin converting enzyme converts angiotensin I to angiotensin II
- Angiotensin II acts on the adrenal cortex’s zona glomerulosa cells to release aldosterone
- Aldosterone acts on the renal distal tubules to retain Na+ and water, thus increasing intravascular volume
- Angiotensin II also acts as a potent arteriolar constrictor and contributes to a rise in BP

46
Q

What factors other than hypotension increase renin secretion?

A

Renin (protease) release is stimulated by increases in:
- Catecholamines *
- Sympathetic activity * through renal nerves
- Prostaglandins *
- Low Na+ states (cardiac failure, liver failure, Na+ depletion)

*1/3 needed to pass

47
Q

What is the role of vasopressin in dehydration?

A
  • Promotes water resorption in collecting ducts via insertion of aquaporins
  • Causes vasoconstriction
48
Q

What hormone systems are involved in the maintenance of extracellular fluid volume?

A
  • Renin-angiotensin-aldosterone system
  • Vasopressin
49
Q

What are the effects of atrial natriuretic peptide in response to fluid overload?

A
  • Increase in Na+ secretion from the kidneys
  • Diuresis
50
Q

What is the normal renal blood flow?

A

1/2 to pass:
- 1.2-1.3L/min
- 25% of CO

51
Q

Describe the factors which determine renal blood flow

A

3/5 to pass:
- Perfusion pressure * (systemic MAP)
- Renal arterial effects (local constriction from NA and angiotensin II; dilation from ACh, prostaglandins and dopamine)
- Renal nerves (sympathetic activation -> constriction -> decreased renal blood flow)
- Autoregulation (myogenic stretch, mediated by NO and angiotensin II)
- Regional differences between cortex and medulla

52
Q

How do blood flow and oxygen extraction vary in different parts of the kidney?

A

2/3 to pass:
- Cortical blood flow is high (5ml/g of tissue) and oxygen extraction is low
- Medullary blood flow is low (2.5ml/g in outer cortex, 0.6ml/g in inner cortex) and oxygen extraction is higher as more metabolic work is being done
- Medulla is vulnerable to hypoxic damage if flow is reduced (low flow, high O2 usage)

53
Q

What are the consequences of a sustained reduction of renal blood flow?

A
  • Renal blood flow is maintained at MAP >70mmHg
  • Medulla is vulnerable to hypoxia (high metabolic rate)
  • ATN
  • Uraemia
54
Q

How can renal blood flow be measured?

A
  1. Fick principle:
    - Amount of substance taken up per unit time divided by arterio-venous concentration difference
  2. PAH (or any substance that is excreted, not metabolised or stored, doesn’t affect flow):
    - Used to measure effective renal plasma flow (90% cleared)
    - ERPF = clearance of PAH = UV/P = 630ml/min
  3. Actual renal plasma flow = ERPF/0.9 = 700ml/min
  4. Renal blood flow = RPF x 1/(1-Hct), where Hct = 0.45
55
Q

What are the major physiological features of acute intrinsic renal failure?

A
  • Loss of urine concentrating and diluting capacity * due to loss of countercurrent mechanism and nephron number
  • Polyuria -> oliguria -> anuria *
  • Uraemia * due to urea and creatinine and toxins (phenol and acids) build up
  • Acidosis *
  • Anaemia
  • Na+ retention *, oedema, heart failure

*3/5 to pass

56
Q

What are common findings in urinalysis of acute intrinsic renal failure?

A
  • Proteinuria
  • Leucocytes
  • Red cells and casts
57
Q

What are urinary casts?

A

Proteinaceous material precipitated in tubules washed into bladder

58
Q

What are the physiological consequences of impaired renal function?

A
  1. Proteinuria (predominantly albuminuria):
    - Due to increased permeability of glomerular capillaries
  2. Uraemia:
    - Accumulation of breakdown products of protein metabolism resulting in symptoms of uraemia
  3. Acidosis:
    - Failure to excrete acid products of digestion/metabolism with urine maximally acidified
    - Total amount of H+ secreted reduced due to impaired renal tubular production of NH4+
    - Exception is in renal tubular acidosis (impaired ability to acidify urine)
  4. Hyperkalaemia:
    - Reduced H+/K+ exchange
  5. Abnormal Na+ handling (retain excess amounts of Na+) via 3 mechanisms:
    - Acute glomerulonephritis: amount of Na+ filtered markedly decreased
    - Nephrotic syndrome: increased aldosterone causes salt retention, low plasma protein means fluid shifts from plasma into interstitium, resulting low plasma volume triggers renin-angiotensin system
    - Volume overload
59
Q

Why does the kidney lose the ability to concentrate and dilute urine in a patient with impaired renal function?

A

In advanced kidney disease, osmolality is fixed at plasma level indicating that the ability to concentrate or dilute urine has been lost
This is due to:
- Disruption of the countercurrent mechanism
- Loss of functioning nephrons (positive feedback in that the increased filtration of the remaining nephrons eventually damages more nephrons from fibrosis)

60
Q
A
61
Q

What conditions increase renin secretion?

A

3 to pass:
- Sodium depletion
- Diuretics
- Hypotension
- Haemorrhage
- Upright position
- Dehydration
- Cardiac failure
- Cirrhosis
- Constriction of renal artery
- Constriction of aorta
- Various psychological stimuli

62
Q

What factors inhibit renin secretion?

A
  • Na+ and Cl- reabsorption
  • Increased BP
  • Angiotensin II
  • Vasopressin
63
Q

What are the physiological effects of dehydration?

A
  • Water loss lowers ECF and ICF leading to decreased BP *, increased HR , increased ADH, decreased GFR and UO *, increased renin/angiotensin, and increased thirst aiming to maintain IV volume
  • In adrenal insufficiency Na+ is lost not only in urine but also into cells

*needed to pass

64
Q

Describe the effects of a rapid IV infusion of 1000ml of normal saline

A
  • Increased Cl- and acidosis
  • Increased baroreceptor firing
  • Decreased HR and increased BP * (Bainbridge reflex described initial increase HR if slow initially)
  • Increased UO
  • Decreased renin/angiotensin
  • Improved capillary return
65
Q

What is an alternative physiological fluid replacement to normal saline?

A

1/2 to pass:
- Hartmann’s (lactated Ringer’s)
- Plasmalyte

66
Q

Where does Na+ reabsorption occur in the nephron?

A
  • Primarily (60%) in the proximal convoluted tubule by Na+/H+ exchange but also a range of co-transport (glucose, AA, lactate)
  • 30% thick ascending limb of loop of Henle via Na+/K+/2Cl- co-transporter, Na+/H+ exchange
  • Nil at thin part of loop of Henle
  • 7% in distal convoluted tubular via NaCl co-transporter
  • 3% collecting ducts through Na+ channels (ENaC)
67
Q

How is Na+ transported from the tubular cell into the interstitium?

A

Na+/K+ ATPase active transport:
- 3x Na+ and 2x K+ across basolateral membrane predominantly into the lateral intercellular spaces

68
Q

Following high Na+ intake, what mechanisms act to enhance Na+ excretion?

A

A slight increase in ECF occurs triggering various mechanisms (2 to pass):
- Stretch receptors in RA and pulmonary veins -> inhibits sympathetic outflow to kidneys -> decreased Na+ reabsorption
- Small increase in arterial pressure -> pressure natriuresis
- Suppression of angiotensin II formation
- Reduced aldosterone secretion secondary to reduced angiotensin II formation
- Stimulation of ANP

69
Q

How does aldosterone influence renal sodium handling?

A
  • Increased tubular reabsorption of Na+, with secretion of K+ and H+ *
  • Latent period of 10-30mins before effect (time delay due to need to alter protein synthesis via action on DNA)
  • Act principally on the collecting ducts to increase number of active epithelial sodium channels

*needed to pass

70
Q

What general mechanisms are involved in renal tubular reabsorption and secretion?

A

Mechanisms involved in reabsorption and secretion include:
- Active transport
- Co-transporters * (secondary active transport)
- Exchangers *
- Ion channels
- Pumps
- Endocytosis
- Passive diffusion and facilitated diffusion

*needed to pass + 1 other

71
Q

What mechanisms in the kidney reduced sodium excretion?

A

Multiple regulatory mechanisms (reflects importance of Na+ as the prime determinant of ECF volume):
1. Reduced GFR *
2. Increased tubular reabsorption:
- Increased adrenocortical hormones, especially aldosterone * (act primarily on collecting ducts via activation of ENaC)
- Decreased ANP (inhibits ENaC)
- Angiotensin II (acting on PCT)
- Decreased secretion of K+ and H+

*needed to pass

72
Q

Describe the juxtaglomerular apparatus

A
  • Afferent and efferent arterioles and tubule touch at one point
  • Macula densa and juxtaglomerular cells
73
Q

Describe the process by which extracellular fluid tonicity is regulated

A

As plasma osmotic pressure rises:
- Sensed via osmoreceptors * in anterior hypothalamus (mainly organum vasculosum of the lamina terminalis, OVLT)
- Thirst increases *
- Vasopressin (ADH) secretion rises * (from posterior pituitary)
- Vasopressin acts on renal V2 receptors resulting in insertion of water channels (aquaporins) * in luminal membranes of renal collecting tubules, allowing more water to return to the body
Conversely as plasma osmotic pressure falls (285mOsm/kg is the critical point), ADH secretion is suppressed

*needed to pass

74
Q

What factors other than rising osmotic pressure increase vasopressin secretion?

A
  • Decreased ECF volume *
  • Pain *
  • Emotion
  • Surgical stress
  • Exercise
  • Nausea and vomiting
  • Standing
  • Angiotensin II
  • Medications (e.g. clofibrate, carbamazepine; alcohol decreases)

*needed to pass + 1 other

75
Q

How does vasopressin act on the kidney?

A
  • In the collecting duct *, ADH binds to G receptor
  • V2 activates adenylyl cyclase
  • Increased intracellular cAMP results in migration of intracellular endosomes
  • Water channels (aquaporin 2 *) inserted into luminal membrane
  • Increased water permeability * results in increased H2O reabsorption

*needed to pass

76
Q

What hormonal changes occur after drinking a large amount of water?

A
  • Begins about 15mins after ingestion, maximum in about 45mins
  • The act of drinking produces a small decrease in ADH secretion resulting in diuresis *
  • Most of the inhibition is produced by the decrease in osmolality * after the water is absorbed

*needed to pass

77
Q

What is thirst, and what causes it?

A

An appetite, under thalamic control:
- Increased plasma osmolality (via osmoreceptors in anterior hypothalamus)
- Hypovolaemia (via renin-angiotensin system, baroreceptors in heart and blood vessels)
- Prandial (learned or habit response, osmolality and GI hormone effects)
- Psychogenic
- Dry pharyngeal mucous membranes

78
Q

What are the actions of vasopressin?

A
  • Retention of water by kidney (collecting duct permeability), thus decreasing blood osmolality
  • V2 receptors -> insertion of aquaporin-2 (water channel proteins stored in endosomes) into cell membranes
  • Decreased cardiac output (via area postrema)
  • Vasoconstriction via V2 receptors
  • Glycogenolysis
  • ACTH secretion from anterior pituitary
79
Q

Describe water handling in the collecting ducts of the kidneys

A
  • The collecting ducts have two portions: a cortical portion and a medullary portion
  • Changes in osmolality and volume in the collecting ducts depend on amount of vasopressin * acting on ducts
  • Vasopressin increased permeability of collecting ducts to water
  • Key to action of vasopressin on the collecting ducts is aquaporin 2: unlike other aquaporins, this is stored in vesicles in cytoplasm of principal cells
  • Vasopressin causes rapid insertion of these vesicles into apical membrane of cells: effect is mediated via V2 receptor, cAMP, protein kinase A, and a molecular motor (one of the dyneins)
  • In presence of enough vasopressin to produce maximal antidiuresis, water moves out of hypotonic fluid entering cortical collecting ducts * into interstitium of cortex, and the tubular fluid becomes isotonic
  • As much as 10% of filtered water is removed
  • When vasopressin is absent, the collecting duct epithelium is relatively impermeable to water and the fluid therefore remains hypotonic, and large amounts flow into renal pelvis

*needed to pass

80
Q

What is an osmotic diuresis?

A
  • Presence of large quantities of unreabsorbed solutes in renal tubules causes an increase in urine volume called osmotic diuresis *
  • Solutes that are not reabsorbed in the proximal tubules exert an appreciable osmotic effect as volume of tubular fluid decreases and their concentration increases: therefore they hold water in the tubules *
  • Result is a marked increase in urine volume, and excretion of Na+ and other electrolytes
  • Osmotic diuresis is produced by administration of compounds such as mannitol and related polysaccharides that are filtered but not reabsorbed
  • It is also produced by naturally occurring substances when present in amounts exceeding the capacity of the tubules to reabsorb them (e.g. glucosuria in diabetes mellitus)
  • Can also be caused by infusion of large amounts of sodium chloride or urea

*needed to pass

81
Q

Describe how water is reabsorbed in the different parts of the nephron

A
  • 60-70% in the proximal tubule
  • 15% in the loop of Henle
  • 5% in the distal tubule
  • Up to 10% in the collecting duct depending on the presence of ADH

ACEM Primary VIVA (45 decks)

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